Killer whales’ diet more important than location for pollutant exposure

Both elegant and fierce, killer whales are some of the oceans’ top predators, but even they can be exposed to environmental pollution. Now, in the largest study to date on North Atlantic killer whales, researchers in ACS’ Environmental Science & Technology report the levels of legacy and emerging pollutants in 162 individuals’ blubber. The animals’ diet, rather than location, greatly impacted contaminant levels and potential health risks — information that’s helpful to conservation efforts.

As the largest member of the dolphin family, killer whales, also known as orcas, are found worldwide. Marine vessel traffic can disturb the hunting and communication of these black-and-white marine mammals. But they face another type of human threat — legacy and emerging persistent organic pollutants (POPs) in their environments. POPs include chlorinated hydrocarbons and flame retardants, and can accumulate in animals’ fat stores as the contaminants move up the food chain though a process called biomagnification.

Previous studies have shown that some Pacific orca populations can carry POP loads in their blubber that pose potential health risks, including reduced immunity, hormonal imbalances and reproductive issues. But information on orcas living in the North Atlantic are lacking. So, Anaïs Remili, Melissa McKinney and colleagues wanted to assess the contaminants present in animals spanning from Eastern Canada to Norway.

The researchers collected skin and blubber biopsies from over a hundred free-ranging killer whales, across the North Atlantic Ocean from Canada, Greenland, Iceland to Norway. They analyzed half of each tissue sample for five classes of POPs, including polychlorinated biphenyls (PCBs). The other portion was used to evaluate the animals’ diets. Multiple features stood out in the data:

  • Specimens from orcas in the western North Atlantic contained substantially higher contaminant loads than ones from orcas on the eastern side — a pattern that contrasts with previously reported POP levels in other Arctic marine organisms.
  • The pattern could be attributed to individuals’ diet rather than location. Specifically, killer whales foraging on fish had the lowest POP levels, and animals consuming marine mammals, such as seals or other whales, had the highest.
  • PCB-associated health risks were highest for killer whales that ate primarily marine mammals, with most animals’ levels exceeding the threshold for a higher risk of female reproductive failure.
  • The levels of one POP, known as α-HBCDD, were the highest reported for any marine mammal to date, despite the fact that this brominated flame retardant was banned a decade ago.

The researchers say the findings support the need for proper waste disposal to prevent contaminants from entering the oceans’ food chains and reaching the top predators. They explain that the findings of their study underscore the need for action to protect North Atlantic killer whales and their ecosystems.

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The NHS must modernise or die, Wes Streeting says

The shadow health secretary warns the ageing population could bankrupt the NHS, as he sets out plans.

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NHS must modernise or die – Streeting tells Labour conference

The shadow health secretary says it is up to Labour to “rescue, rebuild and renew” the NHS.

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Killing remains a threat to Bornean orangutans

University of Queensland research has found despite considerable conservation efforts, the illegal killing of critically endangered orangutans on Borneo may be an ongoing threat to the species.

PhD candidate Emily Massingham from UQ’s Faculty of Science managed a team of researchers which visited 79 villages across the Bornean orangutan range in Kalimantan, conducting face to face interviews with 431 people.

“Our study builds on previous research which indicated killing was one of the key reasons for orangutan population decline, alongside habitat loss,” Ms Massingham said.

“The aim of our project was to understand whether orangutans have been killed in recent times, to look at whether conservation projects are effectively preventing killing, and to gain insights into community perceptions and the motivations behind it.

“It has been almost 15 years since the previous study, and we did not find a clear decrease in killings despite Indonesia’s commendable efforts to reduce habitat loss.

“Thirty per cent of villages reported orangutans had been killed in the last 5 -10 years, despite the practice being both illegal and taboo — which also makes it hard to get an accurate picture of the true scale.”

Ms Massingham said Borneo’s orangutan population had decreased by 100,000 in recent decades, with current estimates suggesting fewer than 100,000 animals remain.

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“Our findings did not indicate that conservation projects are reducing killing, highlighting an urgent need to improve the collective approach to orangutan conservation,” she said.

“Killing by humans needs to be addressed, as our findings suggest it may still be occurring and poses a real threat to the species.”

Ms Massingham said orangutans have long lifespans and breed slowly, so are particularly vulnerable to population declines driven by the death of adult apes.

“Our interviews revealed some of the situations which lead to the killing or displacement of individual orangutans,” she said.

“They include protecting crops and taking infant apes to keep as pets.”

The researchers outlined recommendations that could improve future conservation efforts.

“Working with communities and collaborating across disciplines and projects will be key,” Ms Massingham said.

“Conservationists need to work closely with individual villages to understand their needs and perspectives, identify the social drivers of killing of orangutans and implement solutions that reduce human-orangutan conflict.”

The research was conducted under a RISTEK permit, with the engagement of a local social development organisation to facilitate fieldwork.

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Discovery reveals fragile X syndrome begins developing even before birth

Fragile X syndrome, the most common form of inherited intellectual disability, may be unfolding in brain cells even before birth, despite typically going undiagnosed until age 3 or later.

A new study published today in the journal Neuron by researchers at the University of Wisconsin-Madison showed that FMRP, a protein deficient in individuals with fragile X syndrome, has a role in the function of mitochondria, part of a cell that produces energy, during prenatal development. Their results fundamentally change how scientists understand the developmental origins of fragile X syndrome and suggest a potential treatment for brain cells damaged by the dysfunction.

The study, led by four postdoctoral fellows — Minjie Shen, Carissa Sirois, Yu (Kristy) Guo and Meng Li — working in the lab of the lab of Xinyu Zhao, neuroscience professor and neurodevelopmental diseases researcher a UW-Madison’s Waisman Center, found FMRP regulating a gene called RACK1 to promote mitochondrial function. Using a drug to enhance mitochondrial function, they were able to rescue brain cells damaged by lack of FMRP.

Individuals with FXS may present developmental delays — not sitting, walking or talking at expected ages — as well as mild to severe intellectual disability, learning disabilities and social and behavioral problems. About half are also diagnosed with autism spectrum disorder.

In previous research, Zhao found that mitochondria in mice with an FMRP deficiency that imitates FXS were smaller and unhealthy. Diving deeper, they also discovered that FMRP regulates genes involved in mitochondria fission-fusion, a process into which mitochondria fuse into a bigger shape in order to produce more energy for the cell.

For the study, researchers grew brain cells called neurons grown from induced pluripotent stem cells. Because the stem cells came from people with FXS, the researchers could study the development of the disorder at a cellular level, determining whether mitochondria in human cells experienced issues similar to those in mice.

“And indeed, we found that human neurons also have fragmented (smaller) mitochondria,” Zhao says. They also found fewer mitochondria in neurons derived from FXS patients, which they did not see in the neurons of the mice modeling FXS.

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“In human neurons, it’s a deficit in twofold. Not just fission-fusion, but also likely in the production of mitochondria,” Zhao says.

Although it has been long known that FMRP is deeply involved in FXS, the new discovery pinpoints a role for the protein in early development of the condition.

Symptoms of FXS present long after the baby is born. Many babies appear to be developing typically before showing slower development, autistic features or developmental deficits. Children with FXS are typically diagnosed at three years of age or older.

“Which means many scientists have been thinking that FMRP is more important for the postnatal maturation state,” Zhao says.

FMRP is protein that regulates the use of messenger RNA, sort of a of working copy of DNA used to produce the proteins that make things happen in cells. The researchers found that many of the mRNA strands that interact with FMRP are implicated in autism, providing a molecular link between FXS and autism spectrum disorder. Unexpectedly, many FMRP-bound mRNAs are expressed by genes classified as essential — genes that are very busy during prenatal development but less active after birth.

“This means that FMRP has a function in prenatal development that we have not really thought about before,” Zhao says. “The fact that we found that FMRP also regulates prenatal development is really interesting and is actually indicating that what we see in fragile X syndrome, some of the effects already happened within the prenatal development.”

One of those essential genes is RACK1, identified for the first time as playing a role in FXS.

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“When RACK1 is lower in fragile X neurons, the mitochondria are suffering and the neurons exhibit mitochondrial deficit and hyperexcitability, like immature neurons. But when we reintroduce RACK1, we can rescue this,” Zhao says.

Using cultured neurons derived from individuals with FXS to screen for drugs, the researchers found a drug called leflunomide that corrected mitochondrial deficits. The treatment improved mitochondrial function and reduced the neurons’ hyperexcitability.

Next, Zhao wants to do a detailed biochemical analysis of mitochondrial dysfunction and figure out which key proteins are less present in FXS-affected neurons. She is also working on better understanding how RACK1 and leflunomide work to rescue mitochondrial function.

Other collaborators on the study include Waisman Center investigators Qiang Chang, Anita Bhattacharyya, Andre Sousa, Daifeng Wang, Donna Werling and UW-Madison neuroscience professor Jon Levine.

This research was supported by grants from the National Institutes of Health (R01MH118827, R01NS105200, R01MH116582, R01MH118827, R01HD064743, R01NS064025, R01AG067025, U01MH116492, P51 OD011106, U54HD090256, P50HD105353, R24HD000836 and T32 GM141013) and the Department of Defense (W81XWH-22-1-0621).

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Finding explanation for Milky Way’s warp

The Milky Way is often depicted as a flat, spinning disk of dust, gas, and stars. But if you could zoom out and take an edge-on photo, it actually has a distinctive warp — as if you tried to twist and bend a vinyl LP.

Though scientists have long known through observational data that the Milky Way is warped and its edges are flared like a skirt, no one could explain why.

Now, Harvard astronomers at the Center for Astrophysics | Harvard and Smithsonian (CfA) have performed the first calculations that fully explain this phenomenon, with compelling evidence pointing to the Milky Way’s envelopment in an off-kilter halo of dark matter. The work also bolsters current thinking about how the galaxy evolved and may offer clues into some of the mysteries of dark matter.

The new calculations were led by Jiwon Jesse Han, a Griffin Graduate School of Arts and Sciences student affiliated with the CfA. Published in Nature Astronomy, the work includes co-authors Charlie Conroy and Lars Hernquist, both faculty members at the CfA and in the Department of Astronomy.

Our galaxy is located inside a diffuse cloud called the stellar halo, which extends much farther out into the universe. In groundbreaking work published last year, the Harvard team deduced that the stellar halo is tilted and elliptical in shape, like a zeppelin or football.

Building on that, the team assumed the same shape for the dark matter halo, the larger entity that encompasses everything in and around the Milky Way. Dark matter makes up 80 percent of the galaxy’s mass but is invisible because it doesn’t interact with light, so the shape of that halo must be inferred. Using models to calculate the orbits of stars within a tilted, oblong dark matter halo, the team found a near-perfect match to existing observations of a warped, flared galaxy.

“A tilted dark halo is actually fairly common in simulations, but no one had explored its effect on the Milky Way,” Conroy said. “It turns out that the tilt is an elegant way to explain both the magnitude and direction of our galaxy’s wobbly disk.”

Scientists had long surmised that the Milky Way formed due to a galactic collision; the astronomers’ work further underscores that hypothesis.

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“If the galaxy was just evolving on its own, it would have had this nice, spherical halo, this nice, flat disk,” Han said. “So the fact that the halo is tilted and has a football-like shape suggests that our galaxy experienced a merger event, where two galaxies collide.”

Their calculation of the dark matter halo’s probable shape may also provide clues as to the properties and particle nature of dark matter itself, which remain unsolved mysteries in physics. “The fact that the galaxy is not spherical in our data implies that there is some limit to which dark matter can interact with itself,” Han explained.

Confidence in these findings might lead to better ways to cleverly study the unobservable dark matter that makes up most of the universe. This includes new ways to pick up on kinematic signatures of dark sub-halos, which are miniature dark matter halos zipping around the galaxy.

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Bedbugs: Luton Council deals with 86 bedbug incidents in a year

The council issues advice on how homeowners can deal with bedbugs they may find in their homes

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Bird flu: Scientists see gene editing hope for immune chickens

Researchers have developed gene-edited chickens that are partially resistant to bird flu.

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Partygate revelations destroyed trust in government, inquiry told

Ex-cabinet secretary says ‘under no circumstances’ should lockdown parties have taken place.

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Young children who are close to their parents are more likely to grow up kind, helpful and ‘prosocial’

A loving bond between parents and their children early in life significantly increases the child’s tendency to be ‘prosocial’, and act with kindness and empathy towards others, research indicates.

The University of Cambridge study used data from more than 10,000 people born between 2000 and 2002 to understand the long-term interplay between our early relationships with our parents, prosociality and mental health. It is one of the first studies to look at how these characteristics interact over a long period spanning childhood and adolescence.

The researchers found that people who experienced warm and loving relationships with their parents at age three not only tended to have fewer mental health problems during early childhood and adolescence, but also displayed heightened ‘prosocial’ tendencies. This refers to socially-desirable behaviours intended to benefit others, such as kindness, empathy, helpfulness, generosity and volunteering.

Although the correlation between parent-child relationships and later prosociality needs to be verified through further research, the study points to a sizeable association. On average, it found that for every standard unit above ‘normal’ levels that a child’s closeness with their parents was higher at age three, their prosociality increased by 0.24 of a standard unit by adolescence.

Conversely, children whose early parental relationships were emotionally strained or abusive were less likely to develop prosocial habits over time. The researchers suggest this strengthens the case for developing targeted policies and support for young families within which establishing close parent-child relationships may not always be straightforward; for example, if parents are struggling with financial and work pressures and do not have much time.

The study also explored how far mental health and prosocial behaviour are fixed ‘traits’ in young people, and how far they fluctuate according to circumstances like changes at school or in personal relationships. It measured both mental health and prosociality at ages five, seven, 11, 14 and 17 in order to develop a comprehensive picture of the dynamics shaping these characteristics and how they interact.

The research was undertaken by Ioannis Katsantonis and Dr Ros McLellan, both from the Faculty of Education, University of Cambridge.

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Katsantonis, the lead author and a doctoral researcher specialising in psychology and education, said: “Our analysis showed that after a certain age, we tend to be mentally well, or mentally unwell, and have a reasonably fixed level of resilience. Prosociality varies more and for longer, depending on our environment. A big influence appears to be our early relationship with our parents. As children, we internalise those aspects of our relationships with parents that are characterised by emotion, care and warmth. This affects our future disposition to be kind and helpful towards others.”

The study used data from 10,700 participants in the Millennium Cohort Study, which has monitored the development of a large group of people born in the UK between 2000 and 2002. It includes survey-based information about their prosociality, ‘internalising’ mental health symptoms (such as depression and anxiety) and ‘externalising’ symptoms (such as aggression).

Further survey data provided information about how far the participants’ relationships with their parents at age three were characterised by ‘maltreatment’ (physical and verbal abuse); emotional conflict; and ‘closeness’ (warmth, security and care). Other potentially confounding factors, like ethnic background and socio-economic status, were also taken into account.

The Cambridge team then used a complex form of statistical analysis called latent state-trait-occasion modelling to understand how far the participants’ mental health symptoms and prosocial inclinations seemed to be expressing fixed personality ‘traits’ at each stage of their development. This enabled them, for example, to determine how far a child who behaved anxiously when surveyed was responding to a particular experience or set of circumstances, and how far they were just a naturally anxious child.

The study found some evidence of a link between mental health problems and prosociality. Notably, children who displayed higher than average externalising mental health symptoms at a younger age showed less prosociality than usual later. For example, for each standard unit increase above normal that a child displayed externalising mental health problems at age seven, their prosociality typically fell by 0.11 of a unit at age 11.

There was no clear evidence that the reverse applied, however. While children with greater than average prosociality generally had better mental health at any single given point in time, this did not mean their mental health improved as they got older. On the basis of this finding, the study suggests that schools’ efforts to foster prosocial behaviours may be more impactful if they are integrated into the curriculum in a sustained way, rather than being implemented in the form of one-off interventions, like anti-bullying weeks.

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As well as being more prosocial, children who had closer relationships with their parents at age three also tended to have fewer symptoms of poor mental health in later childhood and adolescence.

Katsantonis said that the findings underlined the importance of cultivating strong early relationships between parents and children, which is already widely seen as critical to supporting children’s healthy development in other areas.

“So much of this comes back to parents,” Katsantonis said. “How much they can spend time with their children and respond to their needs and emotions early in life matters enormously.”

“Some may need help learning how to do that, but we should not underestimate the importance of simply giving them time. Closeness only develops with time, and for parents who are living or working in stressful and constrained circumstances, there often isn’t enough. Policies which address that, at any level, will have many benefits, including enhancing children’s mental resilience and their capacity to act positively towards others later in life.”

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